**Gamma-interferon inhibits Pneumocystis carinii attachment to lung cells by decreasing expression of lung cell-surface integrins**

Authors: POTTRATZ, S. T.; WEIR, A. L.

Source: European Journal of Clinical Investigation, Volume 27, Number 1, January 1997 , pp. 17-22(6)

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Abstract:

Pneumocystis carinii (PC) is a leading cause of pneumonia in immunocompromised patients. Previous work has shown that fibronectin (Fn) and Fn-binding integrins mediate PC attachment to lung cells in vitro. Gamma-interferon (γ-IFN) is a major factor in host defence against PC infection. To determine the effect of γ-IFN on PC attachment to lung cells, the alveolar epithelial cell line A549 was incubated with γ-IFN (0-10⁴ U mL⁻¹) and attachment of ⁵¹Cr-labelled PC to the A549 cells was quantified. PC attachment was significantly decreased (P < 0.01) by addition of γ-IFN with no evidence of injury to either the PC or A549 cells. Effects of γ-IFN on PC attachment were observed after 24 h and reached a maximum after 48 h of incubation. To investigate the mechanism of this decrease, we examined integrin expression on γ-IFN-treated A549 cells. A549 cell expression of the α₅ and β₁ integrin subunits was decreased, whereas expression of the α_v subunit was unchanged. Northern blot analysis showed a similar decrease in mRNA for the α₅ and β₁ integrins. Therefore, γ-IFN-mediated inhibition of PC infection may, in part, result from inhibition of PC attachment to alveolar epithelial cells caused by γ-IFN-induced decreases in alveolar integrin expression.

Keywords: AIDS; cytokine; fibronectin; fibronectin receptor; pneumonia

Document Type: Rapid communication

DOI: http://dx.doi.org/10.1046/j.1365-2362.1997.620612.x

Affiliations: 1: Division of Pulmonary and Critical Care, Indiana University School of Medicine, Indianapolis, IN, USA

Publication date: 1997-01-01